Is the Tako Tsubo syndrome a hyperadrenergic entity?

An interesting case of a young woman presenting the typical features of the syndrome caused by a functional paraganglioma intimate with the aorta and vena cava has been published (3); similar cases of TT syndrome have been reported with adrenal phaeochromocytoma.

Two recent papers reported the findings from endomyocardial biopsies taken during the acute phase of the disease. Both showed histological patterns compatible with strong adrenergic stimulation. In one study 9 patients were biopsied and contraction band necrosis (in 4) and mononuclear cell infiltration (in 3), were documented, associated with elevated levels of norepinephrine and epinephrine peaking on admission (744±52 and 140±166 pg/mc respectively) (4).

Moreover a disproportion between a severely reduced uptake at the ventricular apex on F-18FDG PET image and a slightly reduced uptake of 201 Tl was noted, showing a metabolic defect much more severe than perfusion abnormality (4). Another study performed in TT patients showed intracellular vacuoles of glycogen, disorganisation of contractile and cytoskeletal proteins, while signs of oncotic and apoptotic cell death were absent (5).

After functional recovery of ventricular contractility all described alterations appeared nearly completely reversed. These alterations were interpreted as resulting from catecholamine excess followed by microcirculatory dysfunction and direct cardiotoxicity. A further study performed in 11 consecutive TT patients demonstrated an absence of improvement in contractile performance of the akinetic ventricular wall to low-dose dobutamine infusion (6); a response distinctly different from that expected in an ischemic stunned myocardium, and interpreted as compatible with a catecholamine mediated cardiac toxicity.